Target-specific drug-delivery systems for the administration of pharmaceutical compounds enable the localization of drugs to diseased sites. Various types of drug-delivery systems utilize carriers, such as immunoglobulins, serum proteins, synthetic polymers, liposomes, and microspheres. The vesicular system of niosomes, with their bilayer structure assembled by nonionic surfactants, is able to enhance the bioavailability of a drug to a predetermined area for a period. The amphiphilic nature of niosomes promotes their efficiency in encapsulating lipophilic or hydrophilic drugs. Other additives, such as cholesterol, can be used to maintain the rigidity of the niosomes' structure. This narrative review describes fundamental aspects of niosomes, including their structural components, methods of preparation, limitations, and current applications to various diseases.

Background: Recent human and animal studies have demonstrated the oncostatic properties of N-acetyl-5-methoxytryptamine (melatonin) in different types of cancer. However, in few cancer cell lines including colorectal cancer cell line (HT-29), acute T cell leukemia cell line (JURKAT) and cervical cancer cell line (HeLa), precise oncostatic mechanism induced by melatonin is yet to be described. Objectives: The aim of this study is to investigate the effects of melatonin in HT-29, JURKAT and HeLa cells and to determine the underlying molecular mechanism. Methods: Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay while cell cycle, apoptosis and membrane potential were analysed by flow cytometry. Reactive oxygen species (ROS) was detected by 2',7'.dichlorofluorescein diacetate(DCFH-DA) staining. Protein expressions were determined by Western blot. Results: Our results showed that melatonin suppressed cell proliferation, increased the number of sub G1 hypodiploid cells and cell cycle arrest in HT-29, JURKAT and HeLa cells. Besides, melatonin also induced early and late apoptosis, although there were marked variations in responses between different cell lines (sensitivity; HeLa > HT-29 >JURKAT). Apart from that, staining with DCHF-DA demonstrated ROS production that was induced in a dose-dependent manner in HeLa, HT-29 and JURKAT cells. Moreover, the apoptotic process and oncostatic effect of melatonin were seen to be associated with extracellular-signal-regulated kinase (ERK) and stress-activated protein kinase/c-Jun NH (2)-terminal kinase (SAPK-JNK) signalling cascades in HeLa cells. In HT-29 and JURKAT cells, melatonin induced apoptosis via activation of p38 mitogen-activated protein kinases (p38), ERK and SAPK-JNK signalling pathways. In all three cell lines, the apoptotic event was triggered by the mammalian target of rapamycin (mTOR)-mediated activation of the downstream target rapamycininsensitive companion of mTOR (RICTOR) and/or regulatory-associated protein of mTOR (RAPTOR) proteins. Conclusions: Our findings confirm that melatonin induces apoptosis through reactive oxygen speciesmediated dysregulated mitogen-activated protein kinase (MAPK) and mTOR signalling pathways in these cancer cell lines.